Search bioRxivSearch

bioRxiv · 10.1101/2020.07.11.198390

Anxiety makes time pass quicker: neural correlates

Abstract

Anxiety can be an adaptive process that promotes harm avoidance. It is accompanied by shifts in cognitive processing, but the precise nature of these changes and the neural mechanisms that underlie them are not fully understood. One theory is that anxiety impairs concurrent (non-harm related) cognitive processing by commandeering finite neurocognitive resources. For example, we have previously shown that anxiety reliably speeds up time, promoting temporal underestimation, possibly due to loss of temporal information. Whether this is due anxiety overloading neurocognitive processing of time is unknown. We therefore set out to understand the neural correlates of this effect, examining whether anxiety and time processing overlap, particularly in regions of the cingulate cortex. Across two studies (an exploratory Study 1, N=13, followed by a pre-registered Study 2, N=29) we combined a well-established anxiety manipulation (threat of shock) with a temporal bisection task while participants were scanned using functional magnetic resonance imaging. Consistent with our previous work, time was perceived to pass more quickly under induced anxiety. Anxiety induction led to widespread activation in cingulate cortex, while the perception of longer intervals was associated with more circumscribed activation in a mid-cingulate area. Importantly, conjunction analysis identified convergence between anxiety and time processing in the insula and mid-cingulate cortex. These results provide tentative support for the hypothesis that anxiety impacts cognitive processing by overloading already-in-use neural resources. In particular, overloading mid-cingulate cortex capacity may drive emotion-related changes in temporal perception, consistent with the hypothesised role of this region in mediating cognitive affective and behavioural responses to anxiety.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Ioannis Sarigiannidis, Karel Kieslich, Christian Grillon, Monique Ernst, Jonathan Roiser, Oliver J Robinson. 2020-07-12. Anxiety makes time pass quicker: neural correlates. https://doi.org/10.1101/2020.07.11.198390

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

The Unreasonable Effectiveness of Cell Types in Describing Neuronal Physiological Features

Single-cell RNA sequencing (scRNA-seq) captures detailed gene expression profiles at scale, while patch-clamp recordings measure intrinsic neuronal electrophysiological properties. Modeling the relations between these two modalities remains a challenge. Here, we compare how well electrophysiological features can be predicted by traditional transcriptomic cell type classification, representations derived from a foundational model (scGPT) pretrained on large-scale scRNA-seq datasets, ion channel-coding genes, and highly variable genes. Using paired transcriptomic and electrophysiological patch-sequencing data from 495 human neurons from neurosurgical tissue, we find that cluster-level cell type representations consistently outperform highly variable gene selection, ion channel gene selection, and context-enriched scGPT embeddings. Notably, performance varies across model architectures and initializations, and the best results are obtained by combining the outputs of separate cell type and scGPT-based models. Together, these findings suggest that traditional discrete cellular classification is highly effective in predicting physiological features. For maximum performance it can be complemented by pretrained transformer models.

neuroscience

A nonlinear inhibition pathway underlying cortical responses to tuned holographic optogenetic perturbations

Optogenetics enables causal manipulation of cortical activity. Perturbation responses can be counterintuitive due to network interactions, making theory essential for predicting them. Existing approaches often rely on linear approximations, which fail for many biologically relevant perturbations. Here we develop a nonlinear theory of responses to holographic perturbations in cell-type-specific recurrent networks with structured connectivity. We fit a nonlinear model to mouse V1 data, which shows cotuned-ensemble suppression: perturbing spatially clustered neurons with similar preferred orientations yields markedly stronger short-range suppression than perturbing untuned ensembles. We show that cotuned-ensemble suppression arises from a feature-tuned, nonlinear inhibition pathway implicating somatostatin-positive (SST) interneurons. The theory predicts that cotuned ensembles suppress parvalbumin-positive (PV) neurons but facilitate SST neurons, and links the degree of cotuned-ensemble suppression or facilitation to the variance of the SST response. This framework identifies mechanisms by which nonlinear inhibition sculpts cortical dynamics and establishes a predictive basis for targeted optogenetic interventions.

neuroscience

Proteomic signatures of APOE ε4 across human tissues and cell types in Alzheimers disease

The apolipoprotein E {varepsilon}4 (APOE {varepsilon}4) allele is the strongest genetic risk factor for late-onset Alzheimers disease (AD). However, the underlying molecular mechanisms remain unclear. This study included 1691 participants from the Religious Orders Study and Rush Memory and Aging Project (ROSMAP), 1226 participants from the Accelerating Medicines Partnership - Alzheimers Disease (AMP-AD) Diverse Cohorts Study, and 735 participants from the Alzheimers Disease Neuroimaging Initiative (ADNI). To characterise APOE {varepsilon}4 molecular effects, we analysed proteomic data from plasma, cerebrospinal fluid (CSF), and induced pluripotent stem cell (iPSC)-derived astrocytes and neurons, as well as transcriptomic and proteomic data from multiple brain regions. The association of APOE {varepsilon}4 with AD neuropathology was also examined. APOE {varepsilon}4 carriers shared a plasma proteomic signature enriched for immune processes, irrespective of AD diagnosis. A machine learning classifier trained on this signature discriminated APOE {varepsilon}4 carriers from non-carriers in an independent cohort using CSF proteomics. APOE {varepsilon}4 carriage was associated with higher Braak stages and Consortium to Establish a Registry for Alzheimers Disease (CERAD) score. However, only limited APOE {varepsilon}4-associated transcriptomic and proteomic changes were observed in bulk brain tissue, with poor cross-layer concordance. Proteomic analyses of iPSC-derived astrocytes and neurons further revealed cell-type-specific APOE {varepsilon}4-associated changes. APOE {varepsilon}4 is associated with a consistent proteomic signature across plasma and CSF. Its molecular effects in the brain differ across cell types, brain regions and molecular layers. These findings support the need for cell-type-resolved multi-omic studies to elucidate how APOE {varepsilon}4 confers AD risk.

neuroscience